Ultrastructural changes in hepatic sinusoidal endothelial cells acutely exposed to colloidal iron

被引:4
作者
Bassett, ML
Dahlstrom, JE
Taylor, MC
Koina, ME
Maxwell, L
Francis, D
Jain, S
McLean, AJ
机构
[1] Canberra Hosp, Gastroenterol Unit, Woden, ACT 2606, Australia
[2] Canberra Hosp, Dept Geriatr Med, Woden, ACT 2606, Australia
[3] Univ Sydney, Fac Med, Canberra Clin Sch, Sydney, NSW 2006, Australia
[4] Dept Anat Pathol, Canberra, ACT, Australia
[5] Australian Natl Univ, Canberra Hosp, John Curtin Sch Med Res, Woden, ACT, Australia
[6] Univ Melbourne, Natl Ageing Res Inst, Parkville, Vic, Australia
[7] Univ Melbourne, Royal Melbourne Hosp, Dept Med, Parkville, Vic, Australia
[8] Aged Care Serv, Parkville, Vic, Australia
关键词
hepatic; endothelial; sinusoidal; iron; colloid;
D O I
10.1078/0940-2993-00296
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Hepatic sinusoidal endothelial cells form an important interface between the vascular system, represented by the sinusoids, and the space of Disse that surrounds the hepatocyte microvilli. This study aimed to assess the light microscopic and ultrastructural effects of acute exposure of hepatic sinusoidal endothelial cells to colloidal iron by injection of rats with iron polymaltose. Eight minutes after a single intravenous injection of iron polymaltose sinusoidal endothelial cells showed defenestration, and thickening and layering as assessed by transmission electron microscopy. Kupffer cells and stellate cells appeared activated. These changes were not observed in control animals, experiments using equivalent doses of maltose, or experiments using colloidal carbon except for Kupffer cell activation due to colloidal carbon. No significant light microscopic changes were seen in study or control animals. The findings indicate that acute exposure to colloidal iron causes changes in hepatic sinusoidal endothelial cells, stellate cells and Kupffer cells. This may be the result of a direct toxic effect of iron or increased production of reactive oxygen species. These observations suggest a possible mechanism for defenestration of sinusoidal endothelial cells in ageing and in disease states.
引用
收藏
页码:11 / 16
页数:6
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